FUNCTIONAL-CHANGES IN DORSAL-ROOT GANGLION-CELLS AFTER CHRONIC NERVE CONSTRICTION IN THE RAT

1. We studied the effects of a chronic nerve constriction on the evoke d responses in dorsal root fibers in the rat to norepinephrine and to thermal stimuli applied either to the dorsal root ganglion (DRG) or th e site of nerve injury. We recorded a total of 59 C fibers, 15 A delta -fibers, and 46 A beta-fibers from the L(5) dorsal root of the rats 11 -52 days after a loose ligation of the ipsilateral sciatic nerve. Most fibers were identified by the presence of spontaneous activity (SA) t hat originated partially at and/or proximal to the injury site. In add ition, we recorded 20 C fibers, 1 A delta-fiber, and 28 A beta-fibers from the dorsal roots of normal, uninjured neurons. 2. In nerve-injure d rats, the SA of some C fibers was generally increased by cooling and decreased by heating either site. In contrast, the SA of most A beta- fibers was increased by heating either the injury site or the DRG. Coo ling the DRG decreased SA in A beta-fibers, whereas cooling the injury site typically had no effect. Excitatory responses were not evoked in any fiber group when the same thermal stimuli were applied to the ner ve or DRG tested in normal, uninjured rats. 3. Norepinephrine (<0.5 mM ) applied either to the injury site or the DRG increased the SA of mos t C fibers and A delta-fibers but only a minority of A beta-fibers in previously injured nerves. The threshold concentration for excitation of the DRG somata of C fibers was 0.01 mM. No effects were found for f ibers in uninjured nerves. 4. The effect of norepinephrine was blocked by a pretreatment with yohimbine, an alpha(2)-blocker, but not with p razosin, an alpha(1) blocker. 5. Stimulation of the sympathetic trunk (L(2)-L(3)) excited most C fibers and a minority of A beta-fibers. In contrast, the SA of a minority of C fibers and A beta-fibers was depre ssed during sympathetic stimulation. 6. After a chronic nerve constric tion the DRG becomes a source of abnormal activity modulated by sympat hetically released norepinephrine acting on alpha(2) receptors in DRG somata. This neuropathic activity may contribute to cutaneous pain and hyperalgesia.